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  2. Effects of the TLR4 signaling pathway on apoptosis of neuronal cells in diabetes mellitus complicated with cerebral infarction in a rat model

Effects of the TLR4 signaling pathway on apoptosis of neuronal cells in diabetes mellitus complicated with cerebral infarction in a rat model

  • Sci Rep. 2017 Mar 8;7:43834. doi: 10.1038/srep43834.
Chao Li 1 Li-He Che 2 Tie-Feng Ji 3 Lei Shi 4 Jin-Lu Yu 4
Affiliations

Affiliations

  • 1 Department of Neurology, The First Hospital of Jilin University, Changchun 130021, P.R. China.
  • 2 Department of Infectious Diseases, The First Hospital of Jilin University, Changchun 130021, P.R. China.
  • 3 Department of Radiology, The First Hospital of Jilin University, Changchun 130021, P.R. China.
  • 4 Department of Neurosurgery, The First Hospital of Jilin University, Changchun 130021, P.R. China.
Abstract

This study aims to explore the effects of the TLR4 signaling pathway on the Apoptosis of neuronal cells in rats with diabetes mellitus complicated with cerebral infarction (DMCI). A DMCI model was established with 40 Sprague Dawley rats, which were assigned into blank, sham, DM + middle cerebral artery occlusion (MCAO) and DM + MCAO + TAK242 groups. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. A TUNEL assay was applied for detecting cell Apoptosis, and Western blotting was used for detecting the expression of TLR4, TNF-α, IL-1β and apoptosis-related proteins. Compared with the blank and sham groups, there was an increase in cell Apoptosis, expression of Bcl-2, Bax, cleaved Caspase-3, TNF-α, IL-1β and TLR4 proteins and MDA content and a decrease in SOD activity in the DM + MCAO and DM + MCAO + TAK242 groups. Compared with those in the DM + MCAO group, rats in the DM + MCAO + TAK242 group exhibited an increase in SOD activity and a decrease in cell Apoptosis, expression of Bcl-2, Bax, cleaved Caspase-3, TNF-α, IL-1β and TLR4 proteins and MDA content. Inhibition of the TLR4 signaling pathway reduces neuronal cell Apoptosis and nerve injury to protect the brain.

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